Role of the Insulin-Like Growth Factors in Cancer Development and Progression
Yu and Rohan (1) are to be commended for their comprehensive literature review of the mitogenic and apoptotic actions of insulin-like growth factor (IGF)-I and of the epidemiologic evidence incriminating elevated levels of circulating IGF with excess risks of breast, colorectal, prostate, and other cancers. This evidence is supported by the excess risks of breast and colon cancers in persons with acromegaly that are associated with increased IGF levels (2). In conclusion, Yu and Rohan (1) emphasized "the feasibility and validity of implementing dietary interventions to reduce IGF levels with the goal of preventing cancer."
However, Yu and Rohan appear to be unaware of the fact that, since 1984, most of the nationís milk supply has been contaminated with excess IGF levels resulting from the injection of cows with recombinant bovine growth hormone (rBGH) to increase milk yields (3). Moreover, a substantial proportion of IGF in milk from rBGH-injected cows is in a more bioactive, unbound, protein-free form than is IGF in milk from untreated cows (4). In short-term oral administration experiments in rodents (5,6), IGF resists pasteurization and digestion, is readily absorbed from the gastrointestinal tract, and has growth-promoting effects. Furthermore, converging lines of experimental and epidemiologic evidence (6) have incriminated excess IGF levels in rBGH milk as risk factors for breast and colon cancers. Confirmation of these concerns by an international expert committee prompted the January 2000 European ban on the marketing and sale of rBGH milk (7). Avoidance of rBGH dairy products in favor of natural products would thus appear to be most practical and immediate "dietary intervention to Ö [achieve] the goal of preventing cancer" (1).
Samuel S. Epstein
Correspondence to: Samuel S. Epstein, M.D., University of Illinois, School of Public Health (MC922), 2121 West Taylor St., Chicago, IL 60612-1260 (e-mail: email@example.com).
Journal of the National Cancer Institute, Vol. 93, No. 3, February 7, 2001